The observation that behavioral deficits induced by the deletion of FMRP in the prefrontal cortex during development could then be reversed in the same line of mice after FMRP expression in the adult cortex suggests that (a) the continuous expression of FMRP is needed in the mature CNS for normal brain function, and (b) that viral vector-mediated production of FMRP initiated in adult or young adults might be capable of rescuing at least some aspects of impaired brain function in FXS. The gene discussed is FMR1; the disease is fragile X syndrome.